BURLINGTON, Mass.--(BUSINESS WIRE)--

AlloCure, Inc. today announced that it has initiated a phase 2 clinical trial of AC607, the companys mesenchymal stem cell therapy, as a potential treatment for acute kidney injury (AKI). The randomized, double-blind, placebo-controlled, multi-center trial, designated ACT-AKI (AC607 Trial in Acute Kidney Injury) (NCT01602328), will enroll 200 cardiac surgery subjects at leading tertiary care centers in the United States.

ACT-AKI follows the positive results from a phase 1 AC607 trial in cardiac surgery subjects, which showed an excellent safety profile and encouraging data on the incidence of AKI and hospital length of stay, said Robert M. Brenner, M.D., AlloCure President and Chief Executive Officer. We have worked closely with leaders in the field on the design of ACT-AKI, and trial initiation represents an important milestone for AlloCure and the patients we collectively serve.

AC607 is a promising therapeutic candidate for AKI, for which effective therapies are greatly needed, said Richard J. Glassock, M.D., Emeritus Professor of Medicine at the Geffen School of Medicine at the University of California, Los Angeles. The initiation of ACT-AKI represents a critical step in the development of an innovative therapy for this all-too-common, serious and costly medical condition, for which no approved treatments currently exist beyond supportive care.

About AC607

AC607 is a novel biologic therapy under development for the treatment of AKI. AC607 also possesses potential applications in other grievous illnesses. AC607 comprises allogeneic bone marrow-derived mesenchymal stem cells that are harvested from healthy adult donors and then expanded via a mature and state-of-the art manufacturing process. AC607 homes to the site of injury where it mediates powerful anti-inflammatory and organ repair processes via the secretion of beneficial paracrine factors, without differentiation and repopulation of the injured kidney. Importantly, AC607 avoids recognition by the hosts immune system, enabling administration in an off the shelf paradigm without the need for blood or tissue typing.

About AlloCure

AlloCure, Inc. is a privately held, clinical-stage biotechnology company focused on the treatment of kidney disease. The company is a leader in the AKI field and is pioneering the development of the first effective therapy for the treatment of AKI. The companys headquarters is located in Burlington, MA. For more information about AlloCure, please visit the companys web site at http://www.allocure.com.

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AlloCure Begins Phase 2 Clinical Trial in Acute Kidney Injury

Recommendation and review posted by Bethany Smith

NEW YORK, Sept. 4, 2012 (GLOBE NEWSWIRE) -- NeoStem, Inc. (NYSE MKT:NBS) ("NeoStem" or the "Company"), a rapidly emerging market leader in the fast growing cell therapy market, today announced that Company management will present at three investor conferences in September.

The 19th Annual Newsmakers in the Biotech Industry - BioCentury & Thomson Reuters

Rodman & Renshaw Annual Global Investment Conference

National Investment Banking Association Conference

About NeoStem, Inc.

NeoStem, Inc. continues to develop and build on its core capabilities in cell therapy capitalizing on the paradigm shift that we see occurring in medicine. In particular, we anticipate that cell therapy will have a large role in the fight against chronic disease and in lessening the economic burden that these diseases pose to modern society. We are emerging as a technology and market leading company in this fast developing cell therapy market. Our multi-faceted business strategy combines a state-of-the-art contract development and manufacturing subsidiary, Progenitor Cell Therapy, LLC ("PCT") with a medically important cell therapy product development program, enabling near and long-term revenue growth opportunities. We believe this expertise and existing research capabilities and collaborations will enable us to achieve our mission of becoming a premier cell therapy company.

Our contract development and manufacturing service business supports the development of proprietary cell therapy products. NeoStem's most clinically advanced therapeutic, AMR-001, is being developed at Amorcyte, LLC ("Amorcyte"), which we acquired in October 2011. Amorcyte is developing a cell therapy for the treatment of cardiovascular disease and is enrolling patients in a Phase 2 trial to investigate AMR-001's efficacy in preserving heart function after a heart attack. Athelos Corporation ("Athelos"), which is approximately 80%-owned by our subsidiary, PCT, is collaborating with Becton-Dickinson in the early clinical exploration of a T-cell therapy for autoimmune conditions. In addition, pre-clinical assets include our VSELTM Technology platform as well as our mesenchymal stem cells product candidate for regenerative medicine. Our service business and pipeline of proprietary cell therapy products work in concert, giving us a competitive advantage that we believe is unique to the biotechnology and pharmaceutical industries. Supported by an experienced scientific and business management team and a patent and patent pending (IP) portfolio, we believe we are well positioned to succeed.

Forward-Looking Statements for NeoStem, Inc.

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements reflect management's current expectations, as of the date of this press release, and involve certain risks and uncertainties. Forward-looking statements include statements herein with respect to the successful execution of the Company's business strategy, including with respect to the Company's or its partners' successful development of AMR-001 and other cell therapeutics, the size of the market for such products, its competitive position in such markets, the Company's ability to successfully penetrate such markets and the market for its CDMO business, and the efficacy of protection from its patent portfolio, as well as the future of the cell therapeutics industry in general, including the rate at which such industry may grow. Forward looking statements also include statements with respect to satisfying all conditions to closing the disposition of Erye, including receipt of all necessary regulatory approvals in the PRC. The Company's actual results could differ materially from those anticipated in these forward- looking statements as a result of various factors, including but not limited to (i) the Company's ability to manage its business despite operating losses and cash outflows, (ii) its ability to obtain sufficient capital or strategic business arrangement to fund its operations, including the clinical trials for AMR-001, (iii) successful results of the Company's clinical trials of AMR-001 and other cellular therapeutic products that may be pursued, (iv) demand for and market acceptance of AMR-001 or other cell therapies if clinical trials are successful and the Company is permitted to market such products, (v) establishment of a large global market for cellular-based products, (vi) the impact of competitive products and pricing, (vii) the impact of future scientific and medical developments, (viii) the Company's ability to obtain appropriate governmental licenses and approvals and, in general, future actions of regulatory bodies, including the FDA and foreign counterparts, (ix) reimbursement and rebate policies of government agencies and private payers, (x) the Company's ability to protect its intellectual property, (xi) the company's ability to successfully divest its interest in Erye, and (xii) matters described under the "Risk Factors" in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 20, 2012 and in the Company's other periodic filings with the Securities and Exchange Commission, all of which are available on its website. The Company does not undertake to update its forward-looking statements. The Company's further development is highly dependent on future medical and research developments and market acceptance, which is outside its control.

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NeoStem to Present at Three Investor Conferences in September

Recommendation and review posted by Bethany Smith

September spotlights childhood cancer, which remains the leading cause of death by disease of young Americans. At St. Jude Childrens Research Hospital, doctors and scientists are working to change that statistic

Newswise (MEMPHIS, Tenn. September 4, 2012) As St. Jude Childrens Research Hospital celebrates its 50th anniversary and marks September as Childhood Cancer Awareness Month, investigators are focused on the future.

Although survival rates for childhood cancer have soared to about 80 percent nationally since the hospital opened in 1962, cancer remains the leading cause of death by disease for U.S. children between infancy and age 15. The cause of many childhood cancers remains uncertain. For some cancers, drug development has stalled. For others, successful treatment leaves survivors at increased risk for second cancers and other problems that threaten their health and well-being.

In response to such challenges, St. Jude launched the most ambitious effort yet to identify the causes of some of the most difficult and poorly understood childhood cancers. Known as the St. Jude Childrens Research Hospital Washington University Pediatric Cancer Genome Project, the three-year endeavor is using 21st century technology to decipher the complete normal and cancer genomes of 600 young patients with some of the toughest cancers. The human genome is stored in the DNA found in nearly all cells and provides the instructions needed to assemble and sustain a person.

We expect the Pediatric Cancer Genome Project to catalyze global research in childhood cancer and improve our ability to diagnose, monitor and treat young patients with therapies that target the mutations identified as driving their disease, said Dr. William E. Evans, St. Jude director and chief executive officer. The project is designed to complement larger government efforts focused on adult cancers, which are often quite different from the cancers that strike children and adolescents.

To help realize that goal, published and unpublished whole genome sequencing data from the project are now freely available online to the global scientific community. We hope other researchers will use this rich resource for insight into childhood cancer as well as other diseases of children and adults, said James Downing, M.D., St. Jude scientific director and the projects leader at St. Jude.

The privately funded Pediatric Cancer Genome Project has already yielded remarkable surprises, Downing added. These discoveries are pointing us toward new therapeutic options for children, he said.

The findings include clues to understanding and possibly improving treatment of several cancers, including an aggressive subtype of acute lymphoblastic leukemia (ALL). The subtype is known as early T-cell precursor ALL or ETP-ALL. Although overall long-term survival is now 94 percent for ALL patients treated at St. Jude, the prognosis is much worse for patients with ETP-ALL. The new findings suggest patients in this subgroup might benefit from the addition of drugs developed for treatment of the blood cancer acute myeloid leukemia (AML).

In other studies, Pediatric Cancer Genome Project investigators reported evidence that drugs already under development for adult cancers and other diseases might help in fighting certain childhood tumors. The cancers include the eye tumor retinoblastoma as well as subtypes of the most common childhood brain tumor medulloblastoma.

Pediatric Cancer Genome Project researchers have also identified new mutations at work in an aggressive brain tumor as well as in adolescents and young adults with a tumor of the sympathetic nervous system called neuroblastoma. The results are fueling efforts to find new, more selective therapies for these cancers.

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Gene Sequencing Project Builds the Foundation for Next Generation of Childhood Cancer Care

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 4, 2012) Researchers have discovered two gene variants that raise the risk of the pediatric cancer neuroblastoma. Using automated technology to perform genome-wide association studies on DNA from thousands of subjects, the study broadens understanding of how gene changes may make a child susceptible to this early childhood cancer, as well as causing a tumor to progress.

"We discovered common variants in the HACE1 and LIN28B genes that increase the risk of developing neuroblastoma. For LIN28B, these variants also appear to contribute to the tumor's progression once it forms," said first author Sharon J. Diskin, Ph.D., a pediatric cancer researcher at The Children's Hospital of Philadelphia. "HACE1 and LIN28B are both known cancer-related genes, but this is the first study to link them to neuroblastoma."

Diskin and colleagues, including senior author John M. Maris, M.D., director of the Center for Childhood Cancer Research at Children's Hospital, published the study online Sept. 2 in Nature Genetics.

Striking the peripheral nervous system, neuroblastoma usually appears as a solid tumor in the chest or abdomen. It accounts for 7 percent of all childhood cancers, and 10 to 15 percent of all childhood cancer deaths.

The study team performed a genome-wide association study (GWAS), comparing DNA from 2,800 neuroblastoma patients with that of nearly 7,500 healthy children. They found two common gene variants associated with neuroblastoma, both in the 6q16 region of chromosome 6. One variant is within the HACE1 gene, the other in the LIN28B gene. They exert opposite effects: HACE1 functions as a tumor suppressor gene, hindering cancer, while LIN28B is an oncogene, driving cancer development.

The current study showed that low expression of HACE1, a tumor suppressor gene, and high expression of LIN28B, an oncogene, correlated with worse patient survival. To further investigate the gene's role, the researchers used genetic tools to decrease LIN28B's activity, and showed that this inhibited the growth of neuroblastoma cells in culture.

The new research builds on previous GWAS work by Children's Hospital investigators implicating other common gene variants as neuroblastoma oncogenes. As in the current study, these gene variants show a double-barreled effect, both initiating cancer and provoking its progression.

"In addition to broadening our understanding of the heritable component of neuroblastoma susceptibility, we think this research may suggest new therapies," Diskin added. "Our follow-up studies will focus on how we may intervene on these genes' biological pathways to develop more effective treatments."

Financial support for this study came from the National Institutes of Health (grants CA124709, CA151869, HD026979, and CA136979), the Giulio D'Angio Endowed Chair, the Alex's Lemonade Stand Foundation, Andrew's Army Foundation, the PressOn Foundation, the Abramson Family Cancer Research Institute, Fondazione Italiana per la Lotta al Neuroblastoma and Associazione Italiana per la Ricerca sul Cancro, and the Center for Applied Genomics at The Children's Hospital of Philadelphia. Co-authors with Diskin and Maris included researchers from institutions in Naples, Rende and Rome, Italy.

In addition to their positions at Children's Hospital, both Diskin and Maris are on the faculty of the Perelman School of Medicine at the University of Pennsylvania.

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New gene variants raise risk of neuroblastoma, influence tumor progression

Recommendation and review posted by Bethany Smith

Most random gene expression signatures are significantly associated with breast cancer outcome, according to a research team at Universit Libre de Bruxelles.

The Belgian group, which presented its work in PLoS Computational Biology last year, compared 48 published breast cancer outcome signatures to those comprising random genes and found that 28 of the breast cancer signatures, or 60 percent, were "not significantly better outcome predictors than random signatures of identical size," while 11, or 23 percent, were actually poorer predictors than the median random signature.

These findings prompted a review that appeared in Bioessays this month, as well as a commentary published in June in the journal Breast Cancer Research.

Bertrand Jordan, author of the Bioessays review, called the paper "provocative and iconoclastic," as it "states that many published interpretations of expression profiling experiments are not really significant."

Jordan, who is an emeritus research director at the French National Center for Scientific Research, told BioArray News this week that the paper makes a "strong statement" that "seems to be backed by fairly solid data" and "deserved more exposure than it had received" initially.

In addition to the review and commentary, Vincent Detours, a computational biologist at ULB and corresponding author on the PLoS Computational Biology paper, said that he has received "encouragement" from other researchers since it first appeared.

"My impression is that many people were aware of the issue or felt uncomfortable about the proliferation of signatures, and were pleased to see their concerns addressed," Detours told BioArray News last week.

An 'Iconoclastic' Paper

As Detours noted in an opinion article published last December in The Scientist, the accumulation of signatures with all sorts of biological meaning, but nearly identical prognostic values, had "already looked suspicious" to him, coauthors David Venet and Jacques Dumont, and others as far back as 2007.

After collecting from the literature some signatures with as little connection to cancer as possible, the authors discovered that the signature of the blood cells of Japanese patients who were told jokes after lunch, and a signature derived from the microarray analysis of the brains from mice that suffered social defeat were both associated with breast cancer outcome by any statistical standards.

Link:
'Provocative' Paper Sparks Debate on Relevance of Breast Cancer Gene Expression Signatures

Recommendation and review posted by Bethany Smith

Greg Stock wrote a book about the future of human genetic engineering. (Photo courtesy of Greg Stock.)

While perhaps not yet a majority many parents says they would bioengineer their children if they could, to create the perfect, or more perfect child. Now, that parental dream is closer to reality, but no one is quite sure what the implications may be.

Nearly a decade after the human genome was decoded, scientists are only now beginning to understand its implications.

One of the leading thinkers in this field is the biotech entrepreneurGregory Stock. A biophysicist by training, his 2002 bookRedesigning Humans: Our Inevitable Genetic Futuremakes the case that full-scale genetic engineering is on the way whether we like it or not.

And, Stock believes, if the U.S. doesnt lead the way in developing those advances, other nations will.

Between a third and two-thirds of the population and even higher if you look at China or Thailand and other eastern cultures of parents say if they could enhance the genetics of their children, enhance their either cognitive or physical capabilities, they would absolutely do it," he said.

But engineering traits to improve people remains a thorny issue.

It sounds so compelling, take out a little bit of this, that, its going to be the best of you, Stock said. But actually, we don't have a clue what creates exceptional capabilities."

While Stocks attitude is full-speed ahead, he admits, its going to get weird."

----------------------------------------------------

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Author argues U.S. must lead way on bioengineering

Recommendation and review posted by Bethany Smith

Public release date: 4-Sep-2012 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, September 4, 2012The use of RNA in nanotechnology applications is highly promising for many applications, including the development of new therapeutic compounds. Key technical challenges remain, though, and the challenges and opportunities associated with the use of RNA molecules in nanotechnology approaches are presented in a review article in Nucleic Acid Therapeutics, a peer-reviewed journal from Mary Ann Liebert, Inc. The article is available free online at the Nucleic Acid Therapeutics website.

Peixuan Guo and colleagues, University of Kentucky, Lexington, highlight the ability of RNA to self-assemble into nanoparticles with diverse structures. In "Uniqueness, Advantages, Challenges, Solutions, and Perspectives in Therapeutics Applying RNA Nanotechnology," the authors provide a detailed description of the main challenges faced by the RNA therapeutics industry, including the chemical and thermodynamic instability of the molecules, potential safety and side effect issues, difficulties in delivery and specific targeting, and low yield and high production costs in manufacturing.

"The remarkable structural and enzymatic properties of RNA continue to astound us," says Executive Editor Fintan Steele, PhD, SomaLogic, Inc., Boulder, CO. "It is exciting to see those properties increasingly realized for the benefit of human health and welfare, as described by Dr. Guo and his colleagues."

###

Nucleic Acid Therapeutics is under the editorial leadership of Co-Editors-in-Chief Bruce A. Sullenger, PhD, Duke Translational Research Institute, Duke University Medical Center, Durham, NC, and C.A. Stein, MD, PhD, City of Hope National Medical Center, Duarte, CA; and Executive Editor Fintan Steele, PhD, SomaLogic, Boulder, CO.

About the Journal

Nucleic Acid Therapeutics is an authoritative, peer-reviewed journal published bimonthly in print and online that focuses on cutting-edge basic research, therapeutic applications, and drug development using nucleic acids or related compounds to alter gene expression. Nucleic Acid Therapeutics is the Official Journal of the Oligonucleotide Therapeutics Society. Complete tables of content and a free sample issue may be viewed online at the Nucleic Acid Therapeutics website.

About the Publisher

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Realizing the promise of RNA nanotechnology for new drug development

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5 September 2012

GE not in our best interest

The United States State Department and American multinational companies have been pushing for the release of genetically engineered food into the New Zealand environment at a biotechnology conference being held in Rotorua this week, the Green Party said today.

The ABIC 2012 conference being held in Rotorua is dubbed the World Cup of biotechnology and has seen a huge push from vested interests for GE release into the environment despite public opposition to such a move.

The primary benefactors of Genetic Engineering (GE) are US corporate interests not New Zealand farmers, Green Party primary production spokesperson Steffan Browning said.

The GE focused ABIC 2012 conference in Rotorua this week, is clearly part of a strong push towards GE farming in Aotearoa New Zealand by large multinational companies and Washington.

The US State Department presence at the Rotorua conference shows that pushing GE is part of US foreign policy as much as it is in the interests of big corporates like DuPont and Monsanto.

Consumers around the world dont want a bar of GE and if New Zealand wants to continue reaping the benefits of exporting high value-added produce, we need to steer clear.

GE will not enable more exports it risks locking our produce out of markets and tarnishing our clean green brand. GE is not smart, green economics.

We can add more value to our agricultural exports by leveraging our clean, safe, 100% Pure brand.

View post:
Genetic Engineering not in our best interest

Recommendation and review posted by Bethany Smith

TUESDAY, Sept. 4 (HealthDay News) -- Not only is Internet addiction a legitimate compulsion, it may have the same genetic component as nicotine addiction, a new study suggests.

Out of nearly 850 people interviewed about their Internet habits, German researchers evaluated 132 who showed signs of being hooked to the Web, while another 132 without problematic Internet behavior were selected as a control group.

The addicted users said that all their thoughts revolved around the Internet during the day, and they felt that their well-being was harmed if they couldn't go online. The participants' average age was 25.

The study authors conducted a genetic analysis and discovered that the people with Internet addiction were more likely than others to have a genetic mutation on the CHRNA4 gene, which is known to play a major role in nicotine addiction.

The gene mutation was more common in women with online addiction than in men with the problem, according to the study. But the researchers said further research is needed to confirm this because numerous surveys have found that men are more prone to Internet addiction than women.

The study was recently published in the Journal of Addiction Medicine. The study found an association between the gene mutation and addiction, but it did not prove a definitive link.

Overall, the findings show "that Internet addiction is not a figment of our imagination," study author Christian Montag, of the department for differential and biological psychology at the University of Bonn, said in a university news release.

While more research is needed to further analyze the link between this gene mutation and online addiction, the study "shows that there are clear indications for genetic causes of Internet addiction," Montag said.

Learning more about how genetics influences Internet addiction could lead to better treatments, he noted.

Noting that these addicted Internet users reported only occasional problems in everyday life because of overuse of the Internet, the researchers said extreme users should be evaluated in future research.

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Could Internet Addiction Be Genetic?

Recommendation and review posted by Bethany Smith

Public release date: 4-Sep-2012 [ | E-mail | Share ]

Contact: Dean Forbes dforbes@fhcrc.org 206-667-2896 Fred Hutchinson Cancer Research Center

SEATTLE A team of scientists led by a bone marrow transplant researcher at Fred Hutchinson Cancer Research Center has shed new light on why most bone marrow transplant patients who receive tissue-matched cells from unrelated donors still suffer acute graft-versus-host disease (GVHD). The answer appears to lie in the discovery of previously undetected genetic differences in the DNA of patients and unrelated marrow donors.

The laboratory-based study findings by Effie Petersdorf, M.D., and colleagues soon will be translated to the clinic when a Hutchinson Center transplant protocol the first of its kind opens at Seattle Cancer Care Alliance later this year to test patients and donors for these genetic differences. The goal is to further refine the tissue-matching process to reduce the incidence of GVHD, which affects about 80 percent of patients and has been a longtime, vexing challenge for transplant doctors.

GVHD occurs when the donor immune system (the graft) begins to circulate in the patient's bloodstream and recognizes the host's (the patient's) tissue as foreign. When this happens, the new immune system attacks the recipient's tissues such as the liver, gastrointestinal system and skin.

Bone marrow and stem cell transplants are used to treat a variety of malignant blood diseases such as leukemia. Hematopoietic cell transplantation was pioneered at the Hutchinson Center in the 1970s and continues to be a major focus of research and clinical trials to improve survival and reduce side effects.

Published recently in Science Translational Medicine, the study details how researchers identified two specific single-nucleotide polymorphisms, also called SNPs (pronounced "snips"), within the major histocompatibility complex (MHC) in human DNA that are markers for either acute GVHD or disease-free survival. These markers are distinct from the human leukocyte antigens (HLA), found on the same chromosome as the MHC, that are traditionally used to match recipients and donors, a process called tissue typing.

Researchers found that if a patient and donor have different SNPs, the patient was at increased risk of GVHD or a lower chance of disease-free survival. The scientists surmised that genes located near these SNPs must be involved in that process.

"The question I wanted to ask with this study is whether there could be genes we don't know about that are located close to the major histocompatibility complex that could be influencing GVHD risk," said Petersdorf, a member of the Hutchinson Center's Clinical Research Division. "Now that we know what to test for we can begin screening for the presence of the SNPs in patients and donors and select the optimal donor whose SNP profile will benefit the patient the most."

SNP genotyping is only beneficial for patients when they have multiple matched unrelated donors in order to determine which donor is the optimal match. Fortunately, this is fairly common, according to the study. Of 230 patients who had two or more HLA-matched donors, significant percentages also had at least one donor who was SNP-matched.

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New genetic clues to why most bone marrow transplant patients develop graft-versus-host disease

Recommendation and review posted by Bethany Smith

Discovery will lead to new screening protocol to better match patients & donors

Newswise SEATTLE A team of scientists led by a bone marrow transplant researcher at Fred Hutchinson Cancer Research Center has shed new light on why most bone marrow transplant patients who receive tissue-matched cells from unrelated donors still suffer acute graft-versus-host disease (GVHD). The answer appears to lie in the discovery of previously undetected genetic differences in the DNA of patients and unrelated marrow donors.

The laboratory-based study findings by Effie Petersdorf, M.D., and colleagues soon will be translated to the clinic when a Hutchinson Center transplant protocol the first of its kind opens at Seattle Cancer Care Alliance later this year to test patients and donors for these genetic differences. The goal is to further refine the tissue-matching process to reduce the incidence of GVHD, which affects about 80 percent of patients and has been a longtime, vexing challenge for transplant doctors.

GVHD occurs when the donor immune system (the graft) begins to circulate in the patients bloodstream and recognizes the hosts (the patients) tissue as foreign. When this happens, the new immune system attacks the recipients tissues such as the liver, gastrointestinal system and skin.

Bone marrow and stem cell transplants are used to treat a variety of malignant blood diseases such as leukemia. Hematopoietic cell transplantation was pioneered at the Hutchinson Center in the 1970s and continues to be a major focus of research and clinical trials to improve survival and reduce side effects.

Published recently in Science Translational Medicine, the study details how researchers identified two specific single-nucleotide polymorphisms, also called SNPs (pronounced snips), within the major histocompatibility complex (MHC) in human DNA that are markers for either acute GVHD or disease-free survival. These markers are distinct from the human leukocyte antigens (HLA), found on the same chromosome as the MHC, that are traditionally used to match recipients and donors, a process called tissue typing.

Researchers found that if a patient and donor have different SNPs, the patient was at increased risk of GVHD or a lower chance of disease-free survival. The scientists surmised that genes located near these SNPs must be involved in that process.

The question I wanted to ask with this study is whether there could be genes we dont know about that are located close to the major histocompatibility complex that could be influencing GVHD risk, said Petersdorf, a member of the Hutchinson Centers Clinical Research Division. Now that we know what to test for we can begin screening for the presence of the SNPs in patients and donors and select the optimal donor whose SNP profile will benefit the patient the most.

SNP genotyping is only beneficial for patients when they have multiple matched unrelated donors in order to determine which donor is the optimal match. Fortunately, this is fairly common, according to the study. Of 230 patients who had two or more HLA-matched donors, significant percentages also had at least one donor who was SNP-matched.

A SNP is a base change that involves two or more of the four bases (A, C, T and G) that comprise DNA, and is the simplest form of DNA variation on the human genome. SNPs serve as signposts or markers for nearby genes that are the actual drivers for the effect that they have on disease.

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Researchers Uncover New Genetic Clues to Why Most Bone Marrow Transplant Patients Develop Graft-Versus-Host Disease

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 4, 2012) Fanconi anemia is a recessive genetic disorder affecting 1 in 350,000 babies, which leaves cells unable to repair damaged DNA. This lack of repair puts Fanconi anemia patients at high risk for developing a variety of cancers, especially leukemias and head and neck cancer.

Cruelly, the condition also nixes the use of an entire class of cancer drugs, namely drugs like mitomycin C, by encouraging DNA to crosslink together like sticky strands of bread dough -- generally, healthy cells can repair a few crosslinks whereas cancer cells cannot and so are killed. However, Fanconi anemia patients are unable to repair the damage done to healthy or cancerous cells done by these drugs and so treatment with mitomycin C is frequently fatal.

A University of Colorado Cancer Center study funded by the Fanconi Anemia Research Fund explored the effectiveness of a novel agent in preventing cancer in this population -- namely, resveratrol as found in red wine. The results of this study will be presented at the 24th annual Fanconi Anemia Research Fund Scientific Symposium, September 27-30 at the Grand Hyatt Hotel in Denver, Colo.

In fact, the findings may go far past Fanconi anemia.

"One of the Fanconi genes that is lost is BRCA2 -- the same genetic loss that causes many breast cancers," says Robert Sclafani, PhD, investigator at the University of Colorado Cancer Center and professor of biochemistry and molecular genetics at the CU School of Medicine. "So one mystery is why Fanconi anemia patients don't get breast cancer. In Fanconi, every cell in the body is missing that gene -- Fanconi is a very rare thing but it's telling us something about cancers that aren't so rare."

Sclafani's had already shown the effectiveness of resveratrol in treating head and neck cancer, and in this study explored the effect of resveratrol in Fanconi cell lines -- could it prevent cancer by eliminating the cancer cells in Fanconi patients?

"It turns out that regular Fanconi cells aren't sensitive to resveratrol in the way they're sensitive to drugs like mitomycin C," Sclafani says. Instead, Sclafani hopes that additional mutations found in Fanconi head and neck cancer cells but not in regular Fanconi cells will make the cancer cells sensitive to resveratrol in a way normal Fanconi cells are not. His recent results will be presented at the upcoming meeting.

"It's an interesting population," says Sclafani, "and one that may hold information about many kinds of cancer."

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Rare genetic disease offers insight into common cancers

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Not only have great strides been made in human genetics but also in animal genetics. This is important because such genetic information is not only helpful to the animal, but it frequently can also be applied to humans.

A recent article in the New England Journal of Medicine discussed how genetic research from one type of animal, the dog, has been helpful in better understanding the genetics of certain inherited disorders that are present in both dogs and humans.

It is generally easier to do genetic research on dogs than on people. Dogs reproduce many litters, therefore, more animals are available to study.Compared with dogs who are bred much closer, purebreds, there is more genetic heterogeneity present in humans. This results in a greater number of uncontrolled variables being present in people than in dogs. Such genetic heterogeneity or variables can make it more difficult to interpret the results of genetic studies.

There are many genetic disorders that affect the bones of dogs. Hip dysplasia is frequently found in larger dogs.

Another condition that affects the bones and is also present in both humans and dogs is chondrodysplasia. About 20 breeds of dogs have this condition and as a result they have disproportionately short legs. Examples are dachshunds, corgis and basset hounds.

By studying dogs that are affected with chondrodysplasia, researchers were able to uncover the gene that is responsible for this skeletal abnormality and also the chromosome where it is located.

This information is now being applied to patients with this condition by the geneticists who care for them.

Genetic studies are now underway on dogs who have other human conditions such as cancer, epilepsy, lupus erythematosus and narcolepsy, to name just a few.

But as gene research on humans has been helpful in understanding genetic diseases in people, the same is true of gene research involving animals.

Determining the genetic cause of a disease, be it a human or an animal, brings researchers one big step closer to finding ways to treat and prevent the disorder.

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Dr. Murray Feingold: Animal genetics help scientists understand diseases

Recommendation and review posted by Bethany Smith

Not only have great strides been made in human genetics but also in animal genetics. This is important because such genetic information is not only helpful to the animal, but it frequently can also be applied to humans.

A recent article in the New England Journal of Medicine discussed how genetic research from one type of animal, the dog, has been helpful in better understanding the genetics of certain inherited disorders that are present in both dogs and humans.

It is generally easier to do genetic research on dogs than on people. Dogs reproduce many litters, therefore, more animals are available to study. Compared to dogs who are bred much closer, purebreds, there is more genetic heterogeneity present in humans. This results in a greater number of uncontrolled variables being present in people than in dogs. Such genetic heterogeneity or variables can make it more difficult to interpret the results of genetic studies.

There are many genetic disorders that affect the bones of dogs. Hip dysplasia is frequently found in larger dogs.

Another condition that affects the bones and is also present in both humans and dogs is chondrodysplasia. About 20 breeds of dogs have this condition and as a result they have disproportionately short legs. Examples are dachshunds, corgis and basset hounds.

By studying dogs that are affected with chondrodysplasia, researchers were able to uncover the gene that is responsible for this skeletal abnormality and also the chromosome where it is located.

This information is now being applied to patients with this condition by the geneticists who care for them.

Genetic studies are now underway on dogs who have other human conditions such as cancer, epilepsy, lupus erythematosus and narcolepsy, to name just a few.

But as gene research on humans has been helpful in understanding genetic diseases in people, the same is true of gene research involving animals.

Determining the genetic cause of a disease, be it a human or an animal, brings researchers one big step closer to finding ways to treat and prevent the disorder.

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Feingold: Animal genetics help scientists understand diseases

Recommendation and review posted by Bethany Smith

Rutherford, NJ, Sept. 4, 2012 (GLOBE NEWSWIRE) -- Cancer Genetics, Inc. (CGI), a leader in oncology-focused personalized medicine, today announced that Inc. magazine ranked the company #232 among private Healthcare companies, and #2859 overall on its sixth annual Inc. 500|5000 list, an exclusive ranking of the nation's fastest-growing private companies. The list represents a comprehensive look at the most important segment of the economy--America's independent entrepreneurs. This was the first year the Company has been on the list, and is among the first oncology-focused molecular diagnostic companies on the list.

Panna Sharma, CEO of Cancer Genetics, Inc. says "Our team takes tremendous pride in being among other great companies and in our ability to scale our unique focus on personalizing the diagnosis for cancer patients. This recognition by Inc. results from the dedication of CGI's employees and our commitment towards paving the way of personalized medicine in oncology."

In a stagnant economic environment, median growth rate of 2012 Inc. 500|5000 companies remains an impressive 97 percent. The companies on this year's list report having created over 400,000 jobs in the past three years, and aggregate revenue among the honorees reached $299 billion.

Complete results of the Inc. 5000, including company profiles, methodology and an interactive database that can be sorted by industry, region, and other criteria, can be found at http://www.inc.com/5000.

"Now, more than ever, we depend on Inc. 500/5000 companies to spur innovation, provide jobs, and drive the economy forward. Growth companies, not large corporations, are where the action is," says Inc. editor Eric Schurenberg.

About Cancer Genetics, Inc.

Cancer Genetics, Inc. (CGI) is an emerging leader in the field of personalized medicine, offering products and services that enable cancer diagnostics as well as treatments that are tailored to the specific genetic profile of the individual. CGI is committed to maintaining the standard of clinical excellence through its investment in outstanding facilities and equipment. Our reference laboratory is both CLIA certified and CAP accredited and GLP compliant. In addition we have approvals and accreditations from the states of Florida, Maryland, New York, and New Jersey. The company has been built on a foundation of world-class scientific knowledge and IP in solid and blood-borne cancers, as well as strong research collaborations with major cancer centers such as Memorial Sloan-Kettering and the National Cancer Institute.

For further information, http://www.cancergenetics.com.

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Cancer Genetics, Inc. Named To the 2012 Inc. 500|5000 List

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Mice with olfactory defects can have their sense of smell restored through gene therapy.

D. AUBREY/SCIENCE PHOTO LIBRARY

Gene therapy can fix a defective sense of smell in mice by repairing problems with the hair-like structures on their olfactory neurons, researchers report this week in Nature Medicine1. The study suggests that abnormalities in these structures, called cilia, can be treated, but how the findings can be applied to other organs is unclear.

Cilia are found on the surfaces of many types of cell, and they affect various functions, including sensory perception, movement and cell signaling. Damage to cilia as a result of genetic mutation can cause kidney and liver cysts, extra digits, obesity, blindness and hearing loss in mammals.

The mutations and cellular mechanisms that contribute to such ciliopathies have been well studied, but there's been very little work done in the area of therapeutics, says study leader Jeffrey Martens, a pharmacologist at the University of Michigan in Ann Arbor.

Martens and his colleagues used mice in which a mutant protein causes effects similar to polycystic kidney disease in humans. Mutation of this protein, called intraflagellar transport 88 (IFT88), disrupts cilia expression and function, causing impaired growth, extra digits, blindness and brain abnormalities2. These mice, called Oak Ridge polycystic kidney (ORPK) mice, die by early adulthood.

Because olfactory dysfunction is a common effect of ciliopathy, the researchers examined the olfactory neurons of ORPK mice. In healthy mice, numerous cilia project from the olfactory neurons, but ORPK mice had fewer cilia, and those that remained were shortened and malformed. As expected, these mice also had a deficient sense of smell.

To reverse this defect, the authors inserted a functional IFT88 protein into an adenovirus and then injected the virus into the noses of ORPK mice. The injection restored normal cilia number and structure as well as sense of smell.

Because ORPK mice die young, the authors were unable to conduct behavioural tests in adult mice, but they found that newborn mice injected with IFT88 were better at suckling and feeding both associated with smell. ORPK mice are usually one-quarter the size of normal mice by three weeks of age, but treated pups showed a 60% increase in body weight.

The demonstration that a ciliopathy can be reversed is impressive, says Joseph Gleeson, a neurogeneticist at the University of California, San Diego, but its unclear whether results in the olfactory system will translate to other organs. Olfactory neurons continually regenerate, which is not true of all cells affected by ciliopathies, and some defects may be permanent if cilia do not function correctly during development, Gleeson says.

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Gene therapy restores sense of smell to mice

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BURLINGTON, Mass.--(BUSINESS WIRE)--

AlloCure, Inc. today announced that it has initiated a phase 2 clinical trial of AC607, the companys mesenchymal stem cell therapy, as a potential treatment for acute kidney injury (AKI). The randomized, double-blind, placebo-controlled, multi-center trial, designated ACT-AKI (AC607 Trial in Acute Kidney Injury) (NCT01602328), will enroll 200 cardiac surgery subjects at leading tertiary care centers in the United States.

ACT-AKI follows the positive results from a phase 1 AC607 trial in cardiac surgery subjects, which showed an excellent safety profile and encouraging data on the incidence of AKI and hospital length of stay, said Robert M. Brenner, M.D., AlloCure President and Chief Executive Officer. We have worked closely with leaders in the field on the design of ACT-AKI, and trial initiation represents an important milestone for AlloCure and the patients we collectively serve.

AC607 is a promising therapeutic candidate for AKI, for which effective therapies are greatly needed, said Richard J. Glassock, M.D., Emeritus Professor of Medicine at the Geffen School of Medicine at the University of California, Los Angeles. The initiation of ACT-AKI represents a critical step in the development of an innovative therapy for this all-too-common, serious and costly medical condition, for which no approved treatments currently exist beyond supportive care.

About AC607

AC607 is a novel biologic therapy under development for the treatment of AKI. AC607 also possesses potential applications in other grievous illnesses. AC607 comprises allogeneic bone marrow-derived mesenchymal stem cells that are harvested from healthy adult donors and then expanded via a mature and state-of-the art manufacturing process. AC607 homes to the site of injury where it mediates powerful anti-inflammatory and organ repair processes via the secretion of beneficial paracrine factors, without differentiation and repopulation of the injured kidney. Importantly, AC607 avoids recognition by the hosts immune system, enabling administration in an off the shelf paradigm without the need for blood or tissue typing.

About AlloCure

AlloCure, Inc. is a privately held, clinical-stage biotechnology company focused on the treatment of kidney disease. The company is a leader in the AKI field and is pioneering the development of the first effective therapy for the treatment of AKI. The companys headquarters is located in Burlington, MA. For more information about AlloCure, please visit the companys web site at http://www.allocure.com.

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AlloCure Begins Phase 2 Clinical Trial in Acute Kidney Injury

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Interim results from three patients in an early-stage trial of StemCells Inc's experimental cell treatment for chronic spinal cord injury show that two of them experienced gains in "sensory function," the company said.

StemCells is using neural stem cells, technically adult stem cells, taken from the partly developed brains of fetuses and tested for qualities showing they are destined to form particular types of nerve cells.

The company said that six months after being infused with the cells all three patients have tolerated the transplantation well and there are no safety concerns.

"We clearly need to collect more data to establish efficacy, but we are encouraged," Stephen Huhn, vice president at StemCells, said in a statement. He also said the company is pushing ahead with plans to dose patients with incomplete spinal cord injuries.

The initial phase of the trial involved patients with complete injuries and no neurological function below the level of the spinal injury.

Changes in sensitivity to touch, heat and electrical stimuli were observed in areas below the level of injury in two of the patients, while no changes were seen in the third patient, the company said.

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2 of 3 spinal injury patients see gains in stem cell trial

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Recovery of walking and balance can occur even years after injury in people with incomplete spinal cord injury who participate in locomotor training

Additional study shows patients reduced expenses up to 25% after locomotor training intervention

SHORT HILLS, N.J., Sept. 4, 2012 /PRNewswire-USNewswire/ -- For the first time, new research demonstrates that innovative rehabilitative treatments for individuals with spinal cord injuries can lead to significant functional improvements in patients and a higher quality of life. These treatments are provided through the Christopher & Dana Reeve Foundation NeuroRecovery Network (NRN), a national network of activity-based rehabilitation centers for spinal cord injury. The findings suggest that a shift in both protocol and policy is needed to standardize rehabilitation across multiple centers. The studies were funded by the Reeve Foundation the nation's leading nonprofit dedicated to curing spinal cord injury and improving quality of life for people living with paralysis

(Logo: http://photos.prnewswire.com/prnh/20100511/REEVELOGO )

The NRN is a national network of rehabilitative centers established by the Christopher & Dana Reeve Foundation to translate scientific advances into activity-based rehabilitation treatment for individuals with neurological disorders, and is funded by a cooperative agreement between the Foundation and the U.S. Centers for Disease Control and Prevention (CDC).

Eleven peer-reviewed studies published in the September 2012 issue of Archives of Physical Medicine & Rehabilitation conclude that establishing a network of rehab centers for spinal cord injuries that standardizes treatment can lead to significant functional improvements for chronically injured patients. Using data from a total of 296 patients living with spinal cord injury (SCI) at seven centers across the country, researchers found that the NRN succeeds because of overarching conditions, including:

In addition, one NRN study published in the September issue of Journal of Neurological Physical Therapy found that expenses associated with equipment, home renovations, and transportation decreased by up to 25 percent for both children and adult patients with motor incomplete spinal cord injury due to the function gained following intensive locomotor training intervention.

Locomotor training is an intensive, activity-based intervention therapy that seeks to re-train the nervous system by simulating stepping and walking for those with spinal cord injuries. More than one million people in the U.S. are living with paralysis due to a spinal cord injury according to the Reeve Foundation.

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New Research: Eleven Studies Reveal Individuals with Spinal Cord Injury Experience Improved Health, Function through ...

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Public release date: 4-Sep-2012 [ | E-mail | Share ]

Contact: Debra Kain ddkain@ucsd.edu 619-543-6163 University of California - San Diego

A study led by researchers at the UC San Diego Stem Cell Research program and funded by the California Institute for Regenerative Medicine (CIRM) looks at an important RNA binding protein called LIN28, which is implicated in pluripotency and reprogramming as well as in cancer and other diseases. According to the researchers, their study published in the September 6 online issue of Molecular Cell will change how scientists view this protein and its impact on human disease.

Studying embryonic stem cells and somatic cells stably expressing LIN28, the researchers defined discrete binding sites of LIN28 in 25 percent of human transcripts. In addition, splicing-sensitive microarrays demonstrated that LIN28 expression causes widespread downstream alternative splicing changes variations in gene products that can result in cancer or other diseases.

"Surprisingly, we discovered that LIN28 not only binds to the non-coding microRNAs, but can also bind directly to thousands of messenger RNAs," said first author Melissa Wilbert, a doctoral student in the UC San Diego Biomedical Sciences graduate program.

Messenger RNA or mRNA, are RNA molecules that encode a chemical "blueprint" for the synthesis of a protein. MicroRNAs (miRNAs) are short snippets of RNA that are crucial regulators of cell growth, differentiation, and death. While they don't encode for proteins, miRNAs are important for regulating protein production in the cell by repressing or "turning off" genes.

"The LIN28 protein is linked to growth and development and is important very early in human development," said principal investigator Gene Yeo, PhD, MBA, of the Department of Cellular and Molecular Medicine, the Stem Cell Research Program and the Institute for Genomic Medicine at UC San Diego. "It is usually turned off in adult tissue, but can be reactivated, for instance, in certain cancers or metabolic disorders, such as obesity."

Using genome-wide biochemical methods to look at the set of all RNA molecules across the transcriptome, the researchers found that LIN28 recognizes and binds to a known hairpin-like structure found on the let-7 family of miRNA, but surprisingly, this same structure is also found on mRNAs, allowing LIN28 to directly regulate thousands of targets.

"One of these targets actually encodes for the LIN28 protein itself. In other words, LIN28 helps to make more of itself," said Yeo. This process, known as autoregulation, helps to maintain a so-called "steady-state" system in which a protein positively regulates its own production by binding to a regulatory element of the mRNA for the gene coding it.

"Since these mRNA targets include those known to be involved in gene splicing, we also implicate LIN28 in the regulation of alternative splicing," said Wilbert, adding that abnormal variations in splicing are often implicated in cancer and other disorders.

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Binding sites for LIN28 protein found in thousands of human genes

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MARLBOROUGH, Mass.--(BUSINESS WIRE)--

Advanced Cell Technology, Inc. (ACT; OTCBB: ACTC), a leader in the field of regenerative medicine, announced today that its chief scientific officer, Robert Lanza, M.D., will be delivering the opening Keynote Speech at the 4th Annual Stem Cell Symposium 2012, being held in Singapore, September 6-7. Dr. Lanzas presentation is titled Pluripotent Stem Cells From Benchtop to Clinic.

With the theme, Stem Cell Based Therapy, the symposium will have a particular focus on clinical trials and industrial application of stem cells. Sponsored by Stem Cell Society of Singapore (SCSS), the conference will include scientific presentations from key contributors from academic, clinical, and commercial organizations who are translating basic research on stem cells into therapeutics, with a focus on applying engineering technologies to provide medical solutions.

In their opening statement, the organizers state, We are all keeping our fingers crossed for ACTs success, which will also bring a big boost to the stem cell community.

Other topics of the conference include human induced pluripotent stem cells (hiPSCs), drug screening, adult and cancer stem cells, and stem cell therapies emerging from Asia, with presentations from Indian, Korean and Japanese regenerative medicine companies. There will also be a joint session with the International Society for Cellular Therapy (ISCT) covering important issues concerning the commercialization of stem cells, and addressing issues such as reimbursement, manufacturing, characterization, and clinical implementation issues unique to cell therapies.

About Advanced Cell Technology, Inc.

Advanced Cell Technology, Inc. is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.

Forward-Looking Statements

Statements in this news release regarding future financial and operating results, future growth in research and development programs, potential applications of our technology, opportunities for the company and any other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any statements that are not statements of historical fact (including statements containing the words will, believes, plans, anticipates, expects, estimates, and similar expressions) should also be considered to be forward-looking statements. There are a number of important factors that could cause actual results or events to differ materially from those indicated by such forward-looking statements, including: limited operating history, need for future capital, risks inherent in the development and commercialization of potential products, protection of our intellectual property, and economic conditions generally. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in the companys periodic reports, including the report on Form 10-K for the year ended December 31, 2011. Forward-looking statements are based on the beliefs, opinions, and expectations of the companys management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. Forward-looking statements are based on the beliefs, opinions, and expectations of the companys management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. There can be no assurance that the Companys clinical trials will be successful.

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ACT’s Chief Scientific Officer Dr. Robert Lanza to Deliver Opening Keynote Address at 4th Annual Stem Cell Symposium ...

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GAITHERSBURG, MD--(Marketwire -09/04/12)- Cytomedix, Inc. (CMXI) (CMXI), a fully integrated regenerative medicine company commercializing and developing innovative platelet and adult stem cell technologies, today announced that the Company's AutoloGel System was highlighted in a continuing education program at the Paralyzed Veterans of America Summit 2012 held August 28 to 30 at the Paris Las Vegas Hotel.

The AutoloGel System is a device for the production of autologous platelet rich plasma ("PRP") gel, and is the only PRP device cleared by the U.S. Food and Drug Administration ("FDA") for use in wound management.

The program, titled, "Platelet Rich Plasma (PRP) Gel for Wounds on Persons with SCI," was delivered by Laurie Rappl, PT, DPT, CWS, Clinical Development Liaison for Cytomedix. Ms. Rappl's discussion addressed the underlying mechanisms of action that allow the Company's physiologically relevant concentration of PRP in the AutoloGel System to accelerate healing in recalcitrant wounds in patients with Spinal Cord Injuries ("SCI"), and highlighted the clinical data demonstrating rapid reduction in wound area and volume, as well as reduction of undermining and sinus tracts/tunnels in non-healing wounds in patients with SCI.

"The physiology of SCI -- such as decreased blood flow, blood pressure and blood supply -- causes impairment at every step of the wound healing process. A physiologically relevant concentration of PRP has been shown to improve healing in even the hardest to treat chronic wounds in SCI patients," noted Ms. Rappl.

"It is especially rewarding for Cytomedix to have a continuing education program highlighting the benefits of the AutoloGel System for the treatment of chronic wounds in SCI patients. Pressure ulcers and other chronic wounds are persistent medical challenges that compromise the health and quality-of-life for these paralyzed patients," stated Martin P. Rosendale, Chief Executive Officer of Cytomedix. "Our clinical data demonstrates how the AutoloGel System's physiologically relevant concentration of PRP can rapidly restart the healing process in complex and chronic wounds, including wounds that were recalcitrant to other treatments."

About The Paralyzed Veterans of America SummitParalyzed Veterans' Summit 2012 + EXPO brings together more than 700 healthcare professionals in SCI and multiple sclerosis (MS) care. Doctors, nurses, occupational therapists, physical therapist, social workers and researchers convene to explore and implement holistic strategies to strengthen the continuum of care for SCI and MS patients.

The Paralyzed Veterans of America Summit serves as an educational venue bringing together professionals representing the full spectrum of SCI and MS healthcare and to support clinicians in their pursuit of maintaining their specialty certification and/or license to practice. The objectives are to enhance multi-specialty care across the lifespan of individuals with SCI and MS; to assess advances in the delivery of healthcare services; to present innovative models of care management; to improve practice skills of clinicians, surgeons, researchers and administrators; to discuss evidence-based medicine; to increase the body of knowledge on spinal cord injury and multiple sclerosis, their medical complications and consequences; to promote educational opportunities; to identify research priorities; and to present data on new developments in assessment and treatment.

About Cytomedix, Inc. Cytomedix, Inc. is a fully integrated regenerative medicine company commercializing and developing innovative platelet and adult stem cell separation products that enhance the body's natural healing processes. The Company's advanced autologous technologies offer clinicians a new treatment paradigm for wound and tissue repair. The Company's patient-derived PRP systems are marketed by Cytomedix in the U.S. and distributed internationally. Our commercial products include the AutoloGel System, cleared by the FDA for wound care and the Angel Whole Blood Separation System. The Company is developing novel regenerative therapies using our proprietary ALDH Bright Cell ("ALDHbr") technology to isolate a unique, biologically active population of a patient's own stem cells. A Phase 2 trial evaluating the use of ALDHbr for the treatment of ischemic stroke is underway. For additional information please visit http://www.cytomedix.com.

Safe Harbor StatementStatements contained in this press release not relating to historical facts are forward-looking statements that are intended to fall within the safe harbor rule for such statements under the Private Securities Litigation Reform Act of 1995. The information contained in the forward-looking statements is inherently uncertain, and Cytomedix' actual results may differ materially due to a number of factors, many of which are beyond Cytomedix' ability to predict or control, including among many others, risks and uncertainties related to the Company's reimbursement related efforts, the Company's ability to capitalize on the benefits of the above-referenced CMS determination, the Company's ability to successfully and favorably conclude the negotiations and related discussions with the above-referenced global pharmaceutical company, the Company's ability to successfully integrate the Aldagen acquisition, to successfully manage contemplated clinical trials, to manage and address the capital needs, human resource, management, compliance and other challenges of a larger, more complex and integrated business enterprise, viability and effectiveness of the Company's sales approach and overall marketing strategies, commercial success or acceptance by the medical community, competitive responses, the Company's ability to raise additional capital and to continue as a going concern, and Cytomedix's ability to execute on its strategy to market the AutoloGel System as contemplated. To the extent that any statements made here are not historical, these statements are essentially forward-looking. The Company uses words and phrases such as "believes", "forecasted," "projects," "is expected," "remain confident," "will" and/or similar expressions to identify forward-looking statements in this press release. Undue reliance should not be placed on forward-looking information. These forward-looking statements are subject to known and unknown risks and uncertainties that could cause actual events to differ from the forward-looking statements. More information about some of these risks and uncertainties may be found in the reports filed with the Securities and Exchange Commission by Cytomedix, Inc. Cytomedix operates in a highly competitive and rapidly changing business and regulatory environment, thus new or unforeseen risks may arise. Accordingly, investors should not place any reliance on forward-looking statements as a prediction of actual results. Except as is expressly required by the federal securities laws, Cytomedix undertakes no obligation to update or revise any forward-looking statements, whether as a result of new information, changed circumstances or future events or for any other reason. Additional risks that could affect our future operating results are more fully described in our U.S. Securities and Exchange Commission filings, including our Annual Report on Form 10-K for the year ended December 31, 2011 and other subsequent filings. These filings are available at http://www.sec.gov.

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Cytomedix's AutoloGel System Featured in Continuing Education Program at the Paralyzed Veterans of America Summit 2012

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Editor's Choice Main Category: Ear, Nose and Throat Also Included In: Genetics Article Date: 03 Sep 2012 - 11:00 PDT

Current ratings for: New Discovery Offers Hope For People Who Can't Smell

3.33 (3 votes)

4 (1 votes)

The experts believe that fixing congenital anosmia, which is medical language for not being able to smell anything, may eventually lead to curing similar medical issues which also come from the cilia or small hair-like pieces which reside on the outside of cells and are present in diseases involving the kidneys, eyes, and other parts of the body.

According to the report, it may take a while for the evidence to be able to help humans and it will eventually be extremely significant for individuals who have lost the ability to smell because of some type of medical problem, and not so much for people who can't smell because of trauma to the nose, or simply old age. However, the new findings help researchers to understand anosmia on the cellular level, which gives hope to anyone who does not have a sense of smell that someday their ability to smell may be restored.

Jeffery Martens, Ph.D., senior author of the study commented:

The rodents involved in the study possessed some genetic defect that affected a protein named IFT88. This defect made the individuals have less- than-normal amounts of cilia in their bodies. When this problem occurs in mice, it results in early death and poor feeding habits, while for humans it can be fatal.

IFT88 genes were implanted into the cells in the mice when the researchers gave them a common cold virus which had plenty of normal DNA. This made it easy for the virus to infect them, and therefore, the researchers could insert the virus into the cells of the mice.

After this, the experts were able to analyze the feeding habits of the mice, as well as how they were growing, and the neuron signals which assist in the smelling process.

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New Discovery Offers Hope For People Who Can't Smell

Recommendation and review posted by Bethany Smith

(CBS News) There may be hope for people who are unable to smell. Using gene therapy, scientists have successfully restored the sense of smell in mice that had a genetic mutation that took away their olfactory senses.

Smell disorders or olfactory dysfunction affect one to two percent of people living in North America, according to the National Institute of Deafness and Other Communication Disorders (NIDCD). They partially funded the study along with the National Institute on Diabetes and Digestive and Kidney Diseases (NIDDK), the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and the National Eye Institute (NEI).

However, smell problems increase with age. A study showed that about 25 percent of men between the ages of 60 to 69 and 11 percent of women in that age group had developed a problem with their sense of smell, NIDCD said.

Scientist hypothesize that olfactory dysfunction may be due to a group of genetic disorders called ciliopathies, which include diseases such as polycystic kidney disease and retinitis pigmentosa, an inherited degenerative eye disease that causes severe vision impairment and blindness. Problems with cilia, antenna-like projections on cells that help sense what's around, are the root of these distorders. The cilia are found on olfactory sensory neurons where are located in tissue high up in the nasal cavity in the olfactory system.

In order to see if they could reintroduce the sense of smell, researchers from the University of Michigan tested mice that had a mutated version of the IFT88 gene. When working normally, the gene creates the IFT88 protein which is necessary for the in the development of cilia. Without it, cilia function decreases especially in the olfactory system. The same genetic problem in humans causes congenital anosmia, the inability to smell from birth.

They injected the subjects with an adenovirus - in this case, a version of the common cold virus - with the missing normal IFT88 sequence. Theoretically, it would "infect" the mice's DNA and insert the correct gene into the cells. The mice were given the therapy for three days via the nose and then given 10 days to allow the IFT88 protein to grow.

Two weeks after the three-day treatment, the mice had gained 60 percent of their body weight meaning they were eating more. Often, mice missing the protein are underweight because their lack of smell gives them less motivation to eat. Other tests showed that the neurons connected to smell were working correctly when the mice were exposed to amyl acetate, a strong-smelling chemical also called banana oil.

"Using gene therapy in a mouse model of cilia dysfunction, we were able to rescue and restore olfactory function, or sense of smell," says senior author Jeffrey Martens, an associate professor of pharmacology at University of Michigan, said in a press release. "Essentially, we induced the neurons that transmit the sense of smell to regrow the cilia they'd lost."

The authors said they hope to continue their research on mice who are completely lacking the IFT88 protein and see if there is a way to use the therapy to restore the sense of smell to people who were born with anosmia.

"These results could lead to one of the first therapeutic options for treating people with congenital anosmia," Dr. James F. Battey, Jr., director of the National Institute on Deafness and Other Communications Disorders (NIDCD), said in a press release. "They also set the stage for therapeutic approaches to treating diseases that involve cilia dysfunction in other organ systems, many of which can be fatal if left untreated."

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Scientists restore sense of smell to mice who were born with genetic abnormality

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For the first time, people with broken spines have recovered feeling in previously paralysed areas after receiving injections of neural stem cells.

Three people with paralysis received injections of 20 million neural stem cells directly into the injured region of their spinal cord. The cells, acquired from donated fetal brain tissue, were injected between four and eight months after the injuries happened. The patients also received a temporary course of immunosuppressive drugs to limit rejection of the cells.

None of the three felt any sensation below their nipples before the treatment. Six months after therapy, two of them had sensations of touch and heat between their chest and belly button. The third patient has not seen any change.

"The fact we've seen responses to light touch, heat and electrical impulses so far down in two of the patients is very unexpected," says Stephen Huhn of StemCells, the company in Newark, California, developing and testing the treatment. "They're really close to normal in those areas now in their sensitivity," he adds.

"We are very intrigued to see that patients have gained considerable sensory function," says Armin Curt of Balgrist University Hospital in Zurich, Switzerland, where the patients were treated, and principal investigator in the trial.

The data are preliminary, but "these sensory changes suggest that the cells may be positively impacting recovery", says Curt, who presented the results today in London at the annual meeting of the International Spinal Cord Society.

The patients are the first three of 12 who will eventually receive the therapy. The remaining recipients will have less extensive paralysis.

"The sensory gains, first detected at three months post-transplant, have now persisted and evolved at six months after transplantation," says Huhn. "We clearly need to collect much more data to demonstrate efficacy, but our results so far provide a strong rationale to persevere with the clinical development of our stem cells for spinal injury," he says.

"We need to keep monitoring these patients to see if feeling continues to affect lower segments of their bodies," says Huhn. "These are results after only six months, and we will follow these patients for many years."

Huhn says that the company has "compelling data" from animal studies that the donated cells can repair nerves within broken spines (Neurological Research, DOI: 10.1179/016164106X115116).

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Stem cells bring back feeling for paralysed patients

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